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Unit 2 > Unit 2 - Week 2 - Shillitoe, Stein 4 and 5, and Hanes > Flashcards

Unit 2 - Week 2 - Shillitoe, Stein 4 and 5, and Hanes Flashcards

1
Q

How many genes do parvoviruses have? What are there functions?

A

2 genes: replicative and capsid

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2
Q

How many genes do retroviruses have?

A

About 3 genes

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3
Q

How many genes do papillomaviruses have?

A

About 8 genes

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4
Q

How many genes do adenoviruses have?

A

About 10 genes

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5
Q

How many genes do herpesviruses have?

A

70+ genes

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6
Q

Are viral genes prokaryotic or eukaryotic?

A

Eukaryotic

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7
Q

Gene expression is regulated by _____ TF’s. For example, papillomavirus gene expression is regulated by keratinocyte proteins, and Hebatits B virus gene expression is regulated by liver proteins.

A

Cellular

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8
Q

Give an example of viral genome efficiency.

A

The reading frames for genes can overlap on the same strand and/or on complementary strands.

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9
Q

What percentage of the viral genome encodes for tRNA or protein?

A

100%

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10
Q

True or False: Viruses engage in alternative splicing of RNA.

A

True

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11
Q

When a virus creates a polyprotein, what is necessary to cleave it into individual proteins, and is therefore the target of antiviral drugs?

A

Viral protease, especially important with HIV or Hepatitis C

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12
Q

Give three reasons for the high mutation frequency of viruses:

A
  1. No proofreading/error correction
  2. High error rate of viral polymerase/RDRP
  3. Lake of second strand in some viruses
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13
Q

What are the four types of virus interactions?

A
  1. Complementation
  2. Phenotypic mixing
  3. Recombination
  4. Reassortment
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14
Q

What is viral complementation?

A

If two viruses meet, and one of them is defective at making Y, but the other makes Y, the defective virus can benefit. .

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15
Q

What is viral phenotypic mixing?

A

If two viruses inhabit the same host cell, some of their capsid/coat proteins or phenotypic expression may be shared, but the genomes will remain parentally unique.

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16
Q

True or False: In viral recombination of homologous viruses, progeny are different from their parents.

A

True

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17
Q

Most cells or organisms are only infected with one virus at a time because of:

A
  1. Competition for resources
  2. Blocking of receptors
  3. Stimulation of innate immunity
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18
Q

Name some monogenic disorders that might be treated by viral gene therapy?

A
  1. CF
  2. Retinal disorders
  3. Immune disorders
  4. Liver enzyme deficiencies
  5. Hemophilia
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19
Q

What are some major drawbacks to viral gene therapy?

A

The amount of virus needed to effect a change is 10^10+++

The effects wear off within about 100 days or so.

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20
Q

Independent survival or an organism requires how many genes?

A

At least around 500. Pox is one of the bigger viruses and has about 200.

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21
Q

As with bacteria or humans, viral genes comprise:

A

Enhancer/promoter
Ribosomal entry site
Open reading frame

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22
Q

True or False: DNA and RNA viruses are equally unstable.

A

False. DNA viruses are stable, about 1 mutation per several hundred to thousand generations, whereas RNA viruses are unstable, about 1 mutation per generation.

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23
Q

Fun fact!

A

Host range mutations of measles virus allow it to grow in animal cells and to be harvested for use as a live vaccine. The mutation prevents it from growing in the human vaccine recipient.

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24
Q

______ of influenza viruses make previous vaccines obsolete.

A

Antigenic drift

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25
Q

Name some drug-resistant mutants that have appeared in response to antiviral drugs.

A
  1. Acyclovir-resistant mutants of herpes simplex virus
  2. Protease-inhibitor-resistant mutants of HIV or HCV
  3. Amantadine-resistance of mutant influenza viruses
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26
Q

Give an example of viral complementation.

A

Hepatitis D virus cannot grow without Hepatitis B previousl infection because Hep B expresses a surface protein needed by Hep D.

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27
Q

What is a viral pseudotype?

A

In host cells with more than one virus, sometimes the genome of one virus can get packaged into the capsid of another.

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28
Q

Humans have __1__ polymerase genes while bacteria have only __2__.

A
  1. Three (RNA Pol I, II, III)

2. One

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29
Q

Malignancy is uncontrolled cell growth, often accompanies by significant changes in the __1__ of the cells as the chromosomes change over time. Chromosomes are also useful in establishing __2__.

A
  1. karyotype

2. clonality

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30
Q

In a metastasis, cells become invaseive and migrate to another site. When the move, they retain:

A

Their original cell morphology

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31
Q

What is a sarcoma?

A

Cancer of mesenchymal tissue, like bone, fat, cartilage, muscle

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32
Q

What is carcinoma?

A

Cancer of epitheloid tissue

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33
Q

What is hepatopoietic/lymphoid cancer?

A

Leukemias (WBC from bone marrow) and lymphomas (WBC from spleen and lymph nodes)

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34
Q

What is CIN?

A

Chromosome instability, the gain, loss or rearrangement of chromosomes

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35
Q

What is an oncogene?

A

A dominantly acting gene involved in unregulated cell growth and proliferation

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36
Q

Most oncogenes are carried by:

A

Viruses, which carry them, ie H-ras, rat sarcoma virus
sis - Simian sarcoma virus
abl - Abelson murine leukemia virus

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37
Q

Name come viral oncogenes in humans:

A 
HPV (E6, E7)
EBV - nasopharyngeal cancer, Hodgkin and Burkitt lymphoma
HHV 8 - Kaposi sarcoma
HTLV-1 - T cell leukemia
HTLV-2 - various leukemias
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38
Q

If an oncogene is not transmitted by a virus, what is the alternative way it can take over in a host cell?

A

It converted from a proto-oncogene to a oncogene.

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39
Q

What is a proto-oncogene? Give some examples.

A 
A proto-oncogene is a critically important "housekeeping" gene, many are present throughout the human genome:
Growth factors
Cell surface receptors
Regulation of cell cycle
DNA binding proteins
Intracellular signal transduction
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40
Q

How many mutations in proto-oncogenes are required to cause tumorigenesis? What kind of mutation is this?

A

Only 1 mutation is needed (dominant), this is a gain of fx mutation

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41
Q

The Philadelphia chromosome refers to the genetic marker associated with what cancer?

A

CML, chronic myelogenous leukemia

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42
Q

Explain the chromosomal translocation involved in CML.

A

This is a translocation that occurs between chromosomes 9 and 22, which results in the fusion of a proto-oncogene with a second gene giving rise to a chimeric protein. The result is the loss of properly regulated controls and an overproduction of tyrosine kinase (involved in cell cycle regulation).

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43
Q

The drug Gleevec illustrated the first time:

A

A medication for cancer was developed based on knowledge of the gene mutation and the resultant aberrant protein. In this way, the side effects can be limited because the therapy is targeted.

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44
Q

What is APL?

A

Acute promyelocytic leukemia, a dual fusion 15;17 translocation that breaks the PML gene on 15 and the RARA gene on 17.

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45
Q

The fusion signal created by the t(15;17) of APL can be detected using:

A

FISH

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46
Q

What is a tumor suppressor?

A

A genetic element whose loss or inactivation allows the cell to display an alternate phenotype leading to neoplastic growth. Mutation requires both alleles (recessive)

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47
Q

What are the 2 types of tumor suppressor genes?

A

(1) Gate keepers - suppress tumors by regulating cell cycle or growth inhibition
(2) Caretakers - repair DNA damage, maintain genomic integrity

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48
Q

Caretaker tumor suppressors hava a more _____ effect because their loss of fx may not be directly related to disease.

A

Indirect

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49
Q

Name some normal functions of tumor suppressor genes?

A 
Cell to cell interactions
Regulation of growth inhibitory substances
Cell proliferation
Cell differentiation
Chromosome repair
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50
Q

What is MTS1?

A

Multiple tumor suppressor-1, the second most common tm after p53.

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51
Q

Tumor suppressors are ______, in other words, they only cause disease in one or a few cell types.

A

tissue specific

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52
Q

True or False: Benign tumors will not have chromosome abnormalities like malignant tumors do.

A

False! Benign tumors make have karyotypic changes, while malignant tumors may or may not as well.

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53
Q

Rb1 is the ___1___ mutation and functions as a mitotic checkpoint between ___2___ and ___3___.

A
  1. classic gatekeeper
  2. G1
  3. S
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54
Q

Rb1 is found on chromosome:

A

13q14.2

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55
Q

Rb1 mutation is associated with what cancer?

A

Retinoblastoma

56
Q

What is the onset of disease of Rb and why?

A

Prenatal to 5 years, because once the retina is fully mature, retinoblasts are not transcribed.

57
Q

Explain sporadic vs. inherited retinoblastomas:

A

Sporadic - usually 1 eye (2 somatic mutations) - usually 1 single tumor in 1 eye
Inherited - usually both eyes (1 inherited, 1 somatic) - multiple tumors in both eyes

58
Q

Patients who experience retinoblastoma as a child are more likely to have what complication?

A

Osteosarcoma in their teens

59
Q

If a young person develops a cancer of a tumor suppressor, what does that suggest about the etiology?

A

The first mutation was likely inherited, and the second, a random somatic mutation (Knudson’s Two Hit Hypothesis)

60
Q

Name some common familial cancers.

A 
Breast and ovarian cancer
Familial polyposis colon cancer
Retinoblastima
Wilm's tumor
von Hippel Lindau renal cell cancer
von Recklinghausen neurofibromatosis
61
Q

Li Fraumeni involves an inherited mutation of:

A

p53, no one target tissue, multiple neoplasia

62
Q

BRCA1 is found on chromosome ___1___ near ___2___.

A
  1. 17

2. NF1 and p53

63
Q

BRCA2 is found on chromosome ___1___ near ___2___.

A
  1. 13

2. Rb1

64
Q

True or False: Males with the breast cancer mutation can pass the mutation onto their daughters.

A

True

65
Q

BRCA1 and BRCA2 make up what percentage of familial breast cancer?

A

80-90%, and make up 5-9% of all breast cancer

66
Q

Fanconi anemia, Bloom syndrome, Ataxia Telangectasia, Xeroderma Pigmentosum and Cockayne Syndroma all fall into the category of:

A

Breakage syndromes with bad DNA repair syndromes

67
Q

Chromosome breakage syndromes carry what risks and characteristics?

A

Recessive inheritance
Susceptibility to cancer
Chromosome instability
Defective DNA Repair Mechanism

68
Q

True or False: Sister chromatid exchange is a normal DNA event.

A

True

69
Q

A defect in mismatch repair leads to:

A

2 different cell populations, 1 with the correct sequence and 1 with the mutation.

70
Q

What is microsatellite analysis?

A

DNA repair defects can be detected by microsatellite analysis. Small repeats are present throughout the genome and are highly polymorphic in the population. These are the same technologies used in DNA fingerprinting.

71
Q

Microsattelites are particularly sensitive to DNA damage because:

A

they are subject to replication error due to slippage. A defect in repair can alter the number of repeats

72
Q

HPNCC is ______, it is not ______

A

HPNCC is a normal cellular process gone wrong. It is not a gene mutation that lead to an aberrant protein that lead

73
Q

The primary cancers caused by proto-oncogenes mutatins are:

A

leukemias/lymphomas

74
Q

The primary cancers caused by tumor suppressor mutations are:

A

Solid tumors

75
Q

Proto-oncogene mutations most often have what karyotypical pattern?

A

Chromosome translocation, amplification, (point mutation)

76
Q

Tumor suppressor mutations most often have what karyotypical pattern?

A

Deletions, chromosome loss

77
Q

Chromosome instabilty, or CIN, involves proto-oncogene mutations, tumor suppressor gene mutations, and:

A

Error accumulation (DNA repair defects)

78
Q

As shown in the example of familial polyposis colon cancer, many different mutations arise, either simultaneously (less likely) or in evolutionary succession, but the key to malignancy remains:

A

that they must arise within the same cell. Sequential order is not required. A person with an inherited mutation has a jump start on the process.

79
Q

APC stands for:

A

Adenomatous Polyposis Coli

80
Q

APC is an example of:

A

A tumor suppressor gate keeper gene

81
Q

APC causes

A

The most common forms of colorectal cancer

82
Q

Regarding the clonality seen in cancer, what tool is used to monitor the presence and evolution of clones?

A

Karyotype analysis

83
Q

Increasing complexity and numbers of chromosome abnormalities are associated with:

A

Poorer prognosis, especially at relapse.

84
Q

What is a constitutional karyotype/genotype?

A

The original DNA and chromosome complement that originated in the zygote. Useful for establishing baseline data when tracking chromosomal changes associated with cancers.

85
Q

An acquired anomaly is usually present in ______ cell line

A

a single

86
Q

Karyotype analysis in cancer yields what possible findings?

A

Loss of genetic material - deletion, monosomy
Gain of genetic material - duplication, trisomy, gene amplification
Relocation of genetic material - translocation
**Deletions/duplications may be picked up by FISH

87
Q

True or False: Chromosome findings for leukemia are always unique to the disease:

A

False. If unique, it can point to a specific disease, if general, if can point to a general diagnosis

88
Q

Why are Down Syndrome patients more at risk for developing leukemia?

A

Because trisomy 21 is a genetic anomaly found in leukemia as well.

89
Q

What is “loss of heterozygosity” or LOH?

A

The apparent homozygosity or hemizygosity of tissue which is normally (constitutionally) heterozygous. It is a moleculr tool in determining the presence or absence of a mutation.

90
Q

FISH is extremely useful in monitoring what kinds of cancer patients?

A

Bone marrow transplant patients

91
Q

Allogenic means that a bone marrow transplant was obtained from ___1___. Autologous means that a bone marrow transplant was obtained from __2__.

A
  1. A donor

2. The patient

92
Q

What is the process of bone marrow transplantation?

A
  1. Bone marrow is removed from the pt
  2. Stem cells are collected
  3. Chemotherapy destroys the bone marrow in the pt
  4. Stem cells are stored (frozen)
  5. Stem cells are returned to the bloodstream where they migrate to the bone marrow and re-establish hemapoiesis.
93
Q

What type of stem cell is present in the bone marrow?

A

SSC, somatic stem cell

94
Q

A successful bone marrow transplant shows:

A

Engraftment of the donor cell population and estalblishment of a large, healthy clone. This doesn’t happen if the host’s bad cells outcompete the donor cells. , however, the person can survive with a low level of disease IF the donor cell population remains the majority.

95
Q

The drug herceptin is only effective in what type of breast cancer?

A

HER-2/neu breast cancer, which involves gene amplification, detected by FISH assay

96
Q

BCR-ABL gene rearrangements are associated with:

A

CML (the Philadelphia chromosome)

97
Q

One major function of DNA microarray analysis is:

A

To determine the relatedness between types of diseases

98
Q

What are mutational signatures of human cancer?

A

Using new technology ie DNA seq, scientists were able to perform a large scale study of mutations characteristic of different tumors, and have thus developed unique signature panels that aid in identification purposes. They are not comprehensive, but merely characteristic.

99
Q

When dealing with inherited cancers, risk is correlated to:

A

Number and degree of affected relatives

100
Q

The retinoblastoma tumor suppressor is a function ____ gene

A

recessive

101
Q

Why does retinoblastoma appear to show dominant inheritance?

A

Because family members with the recessive mutation tend to show a proclivity for developing the disease–for some reason there is a high probability of the second mutation occurring.

102
Q

True or false: Leukemia is not inherited.

A

True

103
Q

BRCA1, BRCA1, RB1 and NF1 are all:

A

inherited tumor suppressor genes

104
Q

BRCAa and BRCA2 cancers involve:

A

mutation of DNA repair

105
Q

Eukaryotic mRNA’s are ______ modified.

A

Covalently

106
Q

What is the function of miRNAs (micro RNAs)?

A

To regulate gene expression

107
Q

What is the function of other small RNAs?

A

They are used in RNA splicing, telomere maintenance and other processes.

108
Q

The template strand of DNA is “read” in a:

A

3’ –> 5’ direction, to make 5’ –> 3’ transcriptional (RNA) product

109
Q

What enzymes carry out transcription?

A

RNA Polymerases, they catalyze the formation of phosphodiester bonds that link nucleotides together and form the sugar-phosphate

110
Q

Unlike promotors, terminators are:

A

transcribed (but noncoding)

111
Q

True or False: The transcription start/stop sites are not the same as the start/end of the coding region of a gene.

A

True

112
Q

True or False: Genes are always encoded on the template strand.

A

False: genes can be coded on either Watson or Crick. **Promoter orientation dictates which strand will be transcribed.

113
Q

How are DNA and RNA Polymerases similar?

A

They both make their phosphodiester bonds in the 5 to 3 direction, using the template strand (3-5)

114
Q

How are RNA Polymerases different from DNA polymerases? Name 3 things.

A
  1. RNA Polymerases use NTPs (rNTPs) as substrates, whereas DNA Polymerases use dNTPs
  2. Uracil is the RNA base to DNA’s Thymine
  3. Transcription involves de novo synthesis, thus no primer is required.
  4. RNA Polymerases have no exonuclease functions.
115
Q

Rifampin targets what kind of bacteria, and what kind of structure in that bacteria?

A

TB, mycobacteria, targets RNA Polymerase activity

116
Q

alpha-amanitin inhibits:

A

RNA Pol II, found in mushrooms, toxic, causes cytolysis of hepatocytes

117
Q

What is the function of RNA Pol I?

A

most rRNA genes

118
Q

What is the function of RNA Pol III?

A

tRNA genes, 5S rRNA genes

genes for other small RNAs

119
Q

What is the function of RNA Pol II?

A

Most important, protein-coding genes, some small RNAs, like those in spliceosomes

120
Q

TBP stands for __1__. It’s part of __2__. It is necessary for __3__.

A
  1. TATA Binding Protein
  2. TFIID, a general/basal transcription factor
  3. Pre-initiation complex/beginning of transcription.
121
Q

RNA Pol II must be ____ to leave the promoter and start transcribing mRNA.

A

Phosphorylated

122
Q

General TF’s are required for:

A

Every gene

123
Q

Gene-specific TF’s function to:

A

Turn on a specific gene. They are a requirement.

124
Q

How are mRNAs processed?

A

Co-transcriptionally, and the enzymes necessary are recruited by RNA Pol II

125
Q

In prokaryotes, mRNA is translated when?

A

Cotranscriptionally

126
Q

What are the covalent modifications available to nascent (being born, technically) mRNA?

A

5’-capping

3’polyadenylation

127
Q

Do polyadenylation tails have a DNA template?

A

Nope, they are non-templated.

128
Q

What is the m^7GpppN

A

This is the unusual 5- to 5- linkage of 7-methyl Guanine to RNA as the 5’ cap

129
Q

Why is mRNA covalent modification needed?

A
  1. Transport into the cytoplasm
  2. Increased stability
  3. Translational efficiency
130
Q

What is the process of pre-MRNA splicing?

A

Intron sequences (just the few that are close to splicing branchpoints) are recognized by snRNPs, which cleave the RNA at the intron/exon border and covalently link the exons together.

131
Q

What is a snRNP?

A

small nuclear ribonucleic particles, are RNA-protein complexes that combine with unmodified pre-mRNA and various other proteins to form a spliceosome, a large RNA-protein molecular complex upon which splicing of pre-mRNA occurs.

132
Q

What are the steps involved in pre-mRNA splicing?

A

After the snRNPs assemble, a specific adenine nucleotide in the intron sequence attacks the 5’ splice site and cuts the sugar phosphate backbone of the RNA.
The free 3’ OH sequence of the first exon sequence then reacts with the beginning of the second sequence, which cute the intron at its 3’ end. The lariat containing the intron is released and degraded.

133
Q

Lariat formation results in the branched intrionic RNA having a unique bond. What is that bond?

A

2’ to 5’ phosphodiester linkage

134
Q

What are U-snRNPs?

A

A set of proteins plus a uracil-rich RNA

135
Q

An example of a faulty RNA splicing mechanism can result in what condition?

A

Hutchinson-Gilford Progeria

136
Q

What happens in Hutchinson-Gilford Progeria?

A

A single base change in the DN results in a 50-amino acid deletion in the resulting protein. This base change created a new 5’ splice donor site (mutant)

Unit 2 (11 decks)

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